Smac促凋亡机制及其与肺癌的关系

The mechanism of apoptotic promotion for Smac and lung cancer

由于线粒体蛋白Smac具有促进细胞凋亡作用,因而成为肿瘤研究中重要的凋亡调控因子之一。本文概述了Smac的结构、细胞定位和组织分布;通过Smac与IAPs、TRAIL和其它凋亡调节因子的相互作用,阐述了其促进肿瘤细胞凋亡的作用机制;并从表达、预后和治疗等方面论述了Smac在肺癌中的研究进展。研究表明,Smac表达状况与肺癌的发生发展、预后评估及化疗效果相关。而且,Smac模拟小分子肽能通过级联放大效应增加肺癌细胞化疗敏感性,因此,Smac对肺癌的预后评价和治疗等均有重要的作用。

Since Smac, a mitochondria protein, can promote apoptosis, it becomes one of the most significant apoptosis regulatory factors in the oncology research. This article reviews the structure, cellular localization and tissue distribution of Smac, illustrates its mechanism of action for promoting tumor cell apoptosis by describing the interaction between Smac and IAPs, TRAIL, or other apoptosis regulatory factor, and discusses the research progression of Smac in lung cancer through expression, prognosis and therapy. It is reported that the expression of Smac correlate with development, prognostic evaluation, and chemotherapeutic effectiveness of lung cancer. Besides, a small molecular Smac mimic peptide can improve the sensitivity of chemical therapy in lung cancer cell through cascade amplification effect. Consequently, Smac plays a crucial role in prognostic evaluation and therapy of lung cancer.